| Project/Area Number |
20390172
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Hygiene
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| Research Institution | Mie University |
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Principal Investigator |
OIKAWA Shinji 三重大学, 大学院・医学系研究科, 准教授 (10277006)
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| Co-Investigator(Kenkyū-buntansha) |
YAMASHIMA Tetsumori 金沢大学, 大学院・医学系研究科, 准教授 (60135077)
MURATA Mariko 三重大学, 大学院・医学系研究科, 教授 (10171141)
KATO Takuma 三重大学, 大学院・医学系研究科, 准教授 (60224515)
CHIBA Yoichi 愛知県心身障害者コロニー発達障害研究所, 病理学部, 主任研究員 (30372113)
HIRAKU Yusuke 三重大学, 大学院・医学系研究科, 講師 (30324510)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥18,070,000 (Direct Cost: ¥13,900,000、Indirect Cost: ¥4,170,000)
Fiscal Year 2010: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2009: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2008: ¥6,760,000 (Direct Cost: ¥5,200,000、Indirect Cost: ¥1,560,000)
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| Keywords | パーキンソン病 / 黒質 / 神経細胞死 / 酸化ストレス / 活性酸素種 / 酸化損傷タンパク質 / プロテオミクス解析 / Hsp70 / カルボニル化 / 活性酸素 / 分子シャペロン / 酸化損傷度 |
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| Research Abstract |
Parkinson's disease(PD) is the second most common, chronic age-related neurodegenerative disease. The mechanisms of cell death of dopaminergic neurons in PD have not yet been fully elucidated, but increased oxidative stress is perhaps the most important initiators or mediators of neuronal damage. In this study, to identify target proteins of reactive oxygen species(ROS) oxidation, we investigated oxidative damage of proteins in substantia nigra(SN) isolated from Japanese monkeys after transient cerebral ischemia-reperfusion. The carbonyl levels of molecular chaperones(heat shock 70k Da protein 1, T-complex protein 1 subunit alpha, etc), energy metabolism-related enzymes(mitochondrial aconitase, glutamate dehydrogenase 1, etc) and structural proteins(dihydropyrimidinase-related protein 2, etc) were increased. Therefore, oxidative damage to these proteins in SN may lead to loss of the neuroprotective function, which contributes to neuronal death. Furthermore, carbonylation of these proteins may be used as a biomarker for assessing the neuronal cell death induced by oxidative stress.
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